Aneurysms of the visceral arteries are rare but important vascular lesions. Associated aneurysms are common. Because of the risk of rupture, often with a fatal outcome, an aggressive approach to the treatment of VAA is essential.

This report summarizes our experience with the use of cerebral spinal fluid drainage (CSFD) and naloxone for prevention of postoperative neurologic deficit (paraplegia or paraparesis). Methods: We reviewed 110 consecutive patients with 86 thoracoabdominal aneurysms and 24 thoracic aneurysms. The status of 47 patients (43%) was acute (rupture or dissection), and the status of 52 (47%) was Crawford type I or II. None of the patients had intercostal artery reimplantation. There were two patient groups for analysis of neurologic deficit risk. Group A (61 patients) received naloxone and CSFD, and group B (49 patients) did not. Results: One deficit occurred in group A and 11 deficits occurred in group B (p = 0.001). By multiple logistic regression analysis, the variables acute status, Crawford type II, or group B classification were significant factors for deficit risk. Use of the same logistic regression analysis on the subgroup of 47 patients with acute aneurysms and 33 patients with Crawford type 2 aneurysms confirmed the protective effect of combined CSFD and naloxone (group A) and that clinical presentation and extent of aorta replaced are the primary risk factors for development of deficit. To test this conclusion we developed a highly predictive model (correlation coefficient 0.997 with 16 series of thoracoabdominal aneurysms) for neurologic deficit. We applied our data to this model. Group B had the predicted number of deficits, and group A had substantially fewer deficits than predicted. Conclusions: We conclude that the combined use of CSFD and naloxone offers significant protection from neurologic deficits in patients undergoing thoracoabdominal and thoracic aortic replacement.

Strategies that reduce the volume of spinal fluid drainage but still control spinal fluid pressure are helpful in reducing serious complications. Patients with cerebral atrophy are at increased risk for complications of spinal fluid drainage.

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Infiltration of immunologically active cells into vein grafts is concomitant with the development of intimal hyperplasia (IH) and often leads to obliterative stenosis and graft failure. Previous work has demonstrated the prolonged presence of monocytes and macrophages in vein grafts. The stimuli attracting these macrophages remain unidentified. Monocyte chemotactic protein-1 (MCP-1), a potent and specific chemokine for monocytes/macrophages, is secreted by smooth muscle cells, endothelial cells, fibroblasts, and leukocytes, all of which are present in grafted veins. In this study, we examined the temporal profile of MCP-1 gene expression in rat vein grafts by using reverse transcription-polymerase chain reaction (PCR) and immunohistochemistry. Epigastric vein-to-femoral artery bypass grafts were microsurgically placed and harvested at various time points after grafting. Histological analysis confirmed the consistent development of IH. PCR was performed and relative levels of MCP-1 quantified by autoradiography. Our results show that MCP-1 mRNA levels increased 28-fold by 4 hours after grafting and up to 117-fold by 1 week. After this time MCP-1 mRNA levels decreased; nonetheless, even at 8 weeks after grafting, message levels remained elevated 7-fold above baseline. Immunoreactive MCP-1 protein and ED1+ macrophages were detected at all time points; the degree of immunostaining correlated with MCP-1 mRNA levels. Our results support the hypothesis that upregulation of MCP-1 gene expression in vein grafts results in the recruitment of monocytes and tissue macrophages to the vein wall, which leads to IH. The correlation between monocyte/ macrophage infiltration and IH suggests a critical role for these cells in IH development.